RNase L is a mammalian enzyme that has been implicated in the antiviral effect of the antiviral agent interferon against certain viruses including encephalomyocarditis virus (ECMV), reovirus, and vaccinia virus. It has been shown that treatment of mammalian cells with the antiviral agent interferon induces transcription of the RNase L gene. Treatment with interferon also induces transcription of a set of genes encoding at least four different species of 2-5A synthetase, an enzyme involved in the synthesis of the allosteric effectors that activate the RNase L enzyme. Upon activation, RNase L breaks down both viral and cellular RNA, thus, crippling the ability of the cell to produce progeny virus.
Drugs which activate the RNase L enzyme have the potential to be used as antiviral and cancer chemotherapy agents. Thus, efforts are currently underway to identify antiviral drugs which are capable of specifically and directly stimulating the synthesis of RNase L or the activation of RNase L via the 2-5A system. However, at present there are very few tools which are useful for directly assessing the effect of antiviral drugs that activate RNase L. The most widely used assay is one which monitors the appearance of specific rRNA cleavage products in virus-infected cells following treatment with the drug. However, this assay is difficult and tedious to perform and not always reliable.
Thus, it is desirable to have a new research tool which is useful for determining whether a given antiviral drug is capable of inducing the synthesis or activation of RNase L.